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RBBB does not afect the cardiac axis.
[!TIP] AACT - A2CT => A square CT !
#2021GM-NOV Q18
There are many risk calculators, some region specific. ? Different guideline use different calculators.
Consists of statin therapy and possibly aspirin.
Always given in addition to non pharmacologic measures.
Cutoffs for statin therapy:
Source
These cutoff's are 'consistent with many guidelines' - Source
LDL-C levels should be repeated 6 weeks after initiation of therapy.
[!INFO] Lipid lowering drugs which show no benefit
clofibrate , cholestyramine, or gemfibrozil did not show benefits for these medications on coronary mortality
Benefits of protection Vs. Risk of bleeding is closely matched. (In those without previous ASCVD, Aspirin decreases ASCVD risk but increases bleeding risk).
Needs to be decided on case by case basis along with patient choice.
[[statinIntensity.png]] <- effectiveness of cholesterol lowering drugs
Novel class of lipid lowering drug.
Blocks intestinal absorption of cholesterol by blocking NPC1L1 sterol transporter.
Does not inhibit hepatic cholesterol synthesis or reduce biliary excretion of cholesterol.
Ezetimibe causes a reduction in LDL levels of 13-20%.
Can be coadministered with fenofibrate or HMG-CoA reductase inhibitors, but the recommendation is to dose it at least 2 hours before or 4 hours after taking bile acid sequestrants.
Pupil size is maintained by a balance between sympathetic and parasympathetic tone.
The short ciliary nerve is what carries the post ganglionic parasympathetic neurons.
Isolated oculomotor nerve palsy with pupillary involvement in adults is usually related to compression of the third nerve either by an intracranial aneurysm,typically originating at the junction of the posterior communicating and the internal carotid arteries, or by a pituitary tumor (such as in pituitary apoplexy). Both disorders are life-threatening conditions.
[!INFO] Pressure affects the Parasympathetic nerves
[!INFO] OA isn't just wear and tear
OA is not simply a disease of wear and tear.
Cartilage destruction is a central event but there is definite inflammatory and genetic predisposition as evidenced the identified risk factors and joint prevalence.
OA is considered a disease of the joint, as a whole organ.
Destruction of articular cartilage is a central feature. However, all other joint tissues are affected. (ligaments, tendone, synovium, menisci, subchondral bone, capsule).
Joint cells produce proinflammatory mediates (probably IL-1, IL-6 and TNF) which also stimulate the action of proteases (matrix metalloproteinases MMP) that mediate extracellular matrix destruction.
Sub chondral bone becomes sclerotic (after exposure from destruction of overlying cartilate)
There is a spectrum of disease from
Main categories are localized and generalized:
Initially soft tissue swelling with signs of inflammation.
Several joints will be affected sequentially.
Over years, inflammation settles leaving behind bony nodules on the posterolateral aspect of interphalangeal joints.
DIP more frequently involved than PIP.
Familial
Typical pattern of polyarticular involvement of the hand joints.
Female predomimance, develops around menopause.
Associated with nodal generalized OA (i.e knee, hip, spine OA)
Limited functional impairement.
Fixed adduction of the thumb (squared hand) can occur with OA of the thumb.
Radiological OA may not be symptomatic and may not progress.
There are no medical treatments proven to halt or reverse OA.
(search: jugular venous pressure)
C wave - (?isovolumic) ventricular contraction
X descent - atrial relaxation
Y descent - opening of tricuspid valve. (trycuspid)
Veins which collapse with inspiration suggest a normal JVP. If they don't collapse, JVP is elevated. Source
[!INFO] Kussmaul's sign
Kussmaul's sign: neck veins rise in inspiration rather than fall—often a sign of pericardial tamponade or right heart failure (acute right ventricular myocardial infarction)
[!INFO] Fridrick's sign
Friedrich's sign:Â exaggerated "x" wave or diastolic collapse of the neck veins from constrictive pericarditis.
Some sources say it's the Y descent that's exagerrated.
Source
[!WARNING] Tricuspid regurgitation
TR causes an elevated V wave!: not an elevated C wave like you would expect.
Source
Source
See also
Source
Neprilysin (AKA neutral endopeptidase, NEP) degrades some peptides helpful in heart failure (like ANP, bradykinin etc) and also degrades angiotensin II (which is harmful).
Inhibition of neprilysin is a double edged sword because it causes accumulation of beneficial BNP + others but also deleterious angiotensin II.
Therefore, neprilysin inhibitor is always given together with an angiotensin receptor blocker to minimize the effects of the accumulated angiotensin.
An ACE inhibitor cannot be used instead of the ARB because ACEi and Neprilysin inhibitors both increase bradykinin which can cause angioedema.
Eg: Sacubitril valsartan. (sacubitril is a pro drug
BNP - secreted by ventricles